Calcium-Sensing Receptor on Neutrophil Promotes Myocardial Apoptosis and Fibrosis After Acute Myocardial Infarction via NLRP3 Inflammasome Activation

Ren, Ziqi; Yang, Kai; Zhao, Meng; Liu, Wenxiu; Zhang, Xin; Chi, Jinyu; Shi, Zhiyu; Zhang, Xiaohui; Fu, Yu; Liu, Yue; Yin, Xinhua

doi:10.1016/j.cjca.2019.09.026

Cited by 41 publications

(30 citation statements)

References 29 publications

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“…CaSR in turn activates the NLRP3 inflammasome, resulting in the release of large amounts of IL‐1β from neutrophils, and IL‐1β further upregulates IL‐1R in cardiomyocytes, which eventually leads to cardiomyocyte apoptosis. Inhibition of IL‐1R activation in a model of acute myocardial infarction (AMI) was found to reduce cardiomyocyte apoptosis, which is consistent with the results of clinical studies (Ren et al, 2020).…”

Section: Regulatory Effects Of the Nlrp3 Inflammasome In Primary Cells During Vrsupporting

confidence: 83%

“…Under I/R stress, TXNIP is transported into the cytoplasm, where it inhibits the antioxidant activity of TRX‐1 and activates the NLRP3 inflammasome. This shuttles TXNIP to the mitochondria, where it inhibits TRX‐2 activity, and initiates the death process of cardiomyocytes (Ren et al, 2020; X. Wang et al, 2019; Ye et al, 2017). Furthermore, the increased expression of mitochondrial mitofusins‐2 (Mfn‐2) in cardiomyocytes after I/R injury is also associated with an increase in the levels of markers of NLRP3 inflammasome formation.…”

Section: Regulatory Effects Of the Nlrp3 Inflammasome In Primary Cells During Vrmentioning

confidence: 99%

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The NLRP3 inflammasome: Multiple activation pathways and its role in primary cells during ventricular remodeling

Yan

Yang

et al. 2021

Journal Cellular Physiology

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Inflammasomes are a group of multiprotein signaling complexes located in the cytoplasm. Several inflammasomes have been identified, including NLRP1, NLRP2, NLRP3, AIM2, and NLRC4. Among them, NLRP3 was investigated in most detail, and it was reported that it can be activated by many different stimuli. Increased NLRP3 protein expression and inflammasome assembly lead to caspase‐1 mediated maturation and release of IL‐1β, which triggers inflammation and pyroptosis. The activation of the NLRP3 inflammasome has been widely reported in studies of tumors and neurological diseases, but relatively few studies on the cardiovascular system. Ventricular remodeling (VR) is an important factor contributing to heart failure (HF) after myocardial infarction (MI). Consequently, delaying VR is of great significance for improving heart function. Studies have shown that the NLRP3 inflammasome plays an essential role in the process of VR. Here, we reviewed the latest studies on the activation pathway of the NLRP3 inflammasome, focusing on the effects of the NLRP3 inflammasome in primary cells during VR, and finally discuss future research directions in this field.

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Section: Regulatory Effects Of the Nlrp3 Inflammasome In Primary Cells During Vrsupporting

confidence: 83%

Section: Regulatory Effects Of the Nlrp3 Inflammasome In Primary Cells During Vrmentioning

confidence: 99%

The NLRP3 inflammasome: Multiple activation pathways and its role in primary cells during ventricular remodeling

Yan

Yang

et al. 2021

Journal Cellular Physiology

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“…Confirming these results, the incubation of calindol (a calcium‐sensing receptor agonist) promoted NLRP3 assembly in neutrophils from healthy subjects. The effect was abrogated upon incubation with U73122 (a PLC inhibitor), 2‐APB (an IP3 receptor antagonist), and TG (an ER Ca 2+ ‐ATPase pump inhibitor) or caspase‐1 inhibitor 46 . These results represent a point of novelty, as they suggest a novel mechanism underlying inflammasome activation in innate immune/inflammatory cells and, most importantly, provide a novel potential molecular target for NLRP3 inhibition.…”

Section: Nlrp3 Inflammasome In the Pathophysiology Of Cardiovascular Diseasesmentioning

confidence: 85%

“…In a recent paper, Ren et al 46 showed an increased expression of NLRP3, caspase‐1, and IL‐1β in blood and infiltrated neutrophils from patients after acute MI, that could contribute to ventricular remodeling. In particular, the authors observed that the overactivation of inflammasome signaling in circulating and infiltrating neutrophils resulted from the activation of calcium‐sensing receptors.…”

Section: Nlrp3 Inflammasome In the Pathophysiology Of Cardiovascular Diseasesmentioning

confidence: 99%

NLRP3 inflammasome in cardiovascular diseases: Pathophysiological and pharmacological implications

Pellegrini

Martelli

Antonioli

et al. 2021

Medicinal Research Reviews

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Growing evidence points out the importance of nucleotide‐binding oligomerization domain leucine‐rich repeat and pyrin domain‐containing protein 3 (NLRP3) inflammasome in the pathogenesis of cardiovascular diseases (CVDs), including hypertension, myocardial infarct (MI), ischemia, cardiomyopathies (CMs), heart failure (HF), and atherosclerosis. In this regard, intensive research efforts both in humans and in animal models of CVDs are being focused on the characterization of the pathophysiological role of NLRP3 inflammasome signaling in CVDs. In addition, clinical and preclinical evidence is coming to light that the pharmacological blockade of NLRP3 pathways with drugs, including novel chemical entities as well as drugs currently employed in the clinical practice, biologics and phytochemicals, could represent a suitable therapeutic approach for prevention and management of CVDs. On these bases, the present review article provides a comprehensive overview of clinical and preclinical studies about the role of NLRP3 inflammasome in the pathophysiology of CVDs, including hypertension, MI, ischemic injury, CMs, HF and atherosclerosis. In addition, particular attention has been focused on current evidence on the effects of drugs, biologics, and phytochemicals, targeting different steps of inflammasome signaling, in CVDs.

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“…In the current issue of the Canadian Journal of Cardiology, work from the Yin lab offers an interesting perspective regarding how the calcium-sensing receptor (CaSR)emediated activation of neutrophils affects myocardial remodelling after AMI. 6 The CaSR, a G proteinecoupled receptor, can be activated by increased extracellular Ca 2þ levels to promote assembly of the inflammasome in myeloid cells. 7 After AMI, the extracellular ionic environment is altered owing to cytolysis.…”

Section: Activation Of Neutrophil Inflammasome Is Implicated In Acute Myocardial Infarctionmentioning

confidence: 99%

From Neutrophil Calcium Sensor to Myocardial Remodelling—A Double-Edged Pathway Guided by the Inflammasome

Scott

2020

Canadian Journal of Cardiology

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Calcium-Sensing Receptor on Neutrophil Promotes Myocardial Apoptosis and Fibrosis After Acute Myocardial Infarction via NLRP3 Inflammasome Activation

Cited by 41 publications

References 29 publications

The NLRP3 inflammasome: Multiple activation pathways and its role in primary cells during ventricular remodeling

The NLRP3 inflammasome: Multiple activation pathways and its role in primary cells during ventricular remodeling

NLRP3 inflammasome in cardiovascular diseases: Pathophysiological and pharmacological implications

From Neutrophil Calcium Sensor to Myocardial Remodelling—A Double-Edged Pathway Guided by the Inflammasome

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